Levodopa

Levodopa
Product Name Levodopa
CAS No.: 59-92-7
Catalog No.: CFN99800
Molecular Formula: C9H11NO4
Molecular Weight: 197.20 g/mol
Purity: >=98%
Type of Compound: Phenylpropanoids
Physical Desc.: White powder
Targets: Dopamine D3
Source: The seeds of Mucuna sempervirens Hemsl.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $30/20mg
Levodopa is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), used to treat Parkinson's symptoms.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
  • Front Pharmacol.2021, 12:635510.
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  • Processes2023, 11(2), 385¡£
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    Malays J Med Sci. 2014 Dec;21(Spec Issue):6-11.
    Evaluation of the Cytotoxicity of Levodopa and its Complex with Hydroxypropyl-ß-Cyclodextrin (HP-ß-CD) to an Astrocyte Cell Line.[Pubmed: 25941458]

    METHODS AND RESULTS:
    A simple, reliable a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxy-phenyl)-2-(4-sulfophenyl)-2H-tetrazolium, (MTS) assay was conducted to evaluate the potential cytotoxic effects of Levodopa, a "gold standard therapy" for Parkinsonism, and its complex with Hydroxypropyl-β-Cyclodextrin (HP-β-CD) on an astrocyte cell line. The cells were incubated in a range of concentrations from 4.69 to 300 μg/mL Levodopa, HP-β-CD or the complex for up to 72 hours. At every 24-hour interval, the optical density (OD), which reflects the number of viable cells, was recorded. In general, linear dose-dependent cytotoxicity profiles were observed for the cells subjected to Levodopa or the complex, whereas a slightly triphasic response was observed for the cells exposed to HP-β-CD. A significant difference (P < 0.05) in cytotoxicity was detected between the HP-β-CD-treated group and the Levodopa-treated group.
    CONCLUSIONS:
    In particular, we observed that the cells treated with the complex, even at the highest concentrations (> 200 μg/mL), exhibited improved tolerability in a time-dependent manner, which may indicate the potential ability of HP-β-CD to mask the toxic effects of Levodopa via complexation.
    Zhonghua Yi Xue Za Zhi. 2015 Feb 17;95(7):493-5.
    [Effects of a single dose levodopa on heart rate variability in Parkinson's disease].[Pubmed: 25916922]
    To explore the effects of Levodopa on heart rate variability (HRV) in Parkinson's disease (PD).
    METHODS AND RESULTS:
    A total of 48 PD patients (M:F = 35: 13, mean age: 59 ± 6 years, duration of illness: 4.7 ± 1.8 years, Hoehn & Yahr stage: 2.2 ± 0.3) on a stable dose of Levodopa were recruited from January 2012 to May 2014.For confirming autonomic dysfunction, the baseline patient data (12 hours off-medication) were compared with a control group consisting of 48 age and gender-matched healthy subjects (M: F = 35: 13, mean age 58 ± 6 years). Resting lead II electrocardiogram (ECG) was recorded at baseline and continuously after two tablets of 100/10 mg Levodopa/carbidopa.However, 5-min segments were selected from every quarter, i.e., Q1 (0-15 min), Q2 (15-30 min), Q3 (30-45 min) and Q4 (45-60 min). Artifact-free 5-min segments of ECG were analyzed offline to acquire the parameters of heart rate variability in time and frequency domains. At baseline, PD patients had a significantly reduced standard deviation of normal-to-normal intervals (SDRR) [(24 ± 4) vs (26 ± 4) ms, P < 0.01)] and total power (TP) [(569 ± 180) vs (652 ± 205) ms2, P < 0.05] when compared to controls. Comparing of HRV in PD patients at baseline and during first hour after drug administration, we observed significant increase in SDRR [(29 ± 12) vs (24 ± 8) ms, P < 0.05)], TP [(708 ± 253) vs (569 ± 180) ms2, P < 0.01], low frequency power (LF) [(203 ± 98) vs (168 ± 60) ms2, P < 0.05) ] and high frequency power (HF) [158 ± 86) vs (114 ± 90) ms2, P < 0.05] in Q3.
    CONCLUSIONS:
    The results suggest an improvement in the overall variability of heart rate resulting from an enhanced vagal tone.
    Physiol Behav. 2015 Apr 23;147:193-197.
    Coadministration of hydroxysafflor yellow A with levodopa attenuates the dyskinesia.[Pubmed: 25914172]
    Levodopa (L-DOPA) is used as the most effective drug available for the symptomatic treatment of Parkinson's disease (PD). However, long-term treatment of Levodopa frequently causes complications, including abnormal involuntary movements such as dyskinesia and response fluctuations in PD patients.
    METHODS AND RESULTS:
    In the present work, we investigated whether hydroxysafflor yellow A (HSYA) ameliorates Levodopa-induced dyskinesia and motor fluctuations in the 6-hydroxydopamine-lesioned rat model of PD. Valid PD rats were treated daily with vehicle, HSYA alone, Levodopa, or a combination of HSYA plus Levodopa for 21days, respectively.Levodopa(8mg/kg) and benserazide (15mg/kg) were treated intraperitoneally. HSYA was administrated intraperitoneally at a dose of 10mg/kg. The abnormal involuntary movements and rotational behavior were evaluated. The expression of the dopamine D3 receptor in the striatum was also assayed. The results demonstrated that daily administration of Levodopa to PD rats for 21days induced a steady expression of dyskinesia. Coadministration of HSYA with Levodopa significantly ameliorated Levodopa-induced dyskinesia. The combination treatment also prevented the shortening of the motor response duration that defines wearing off motor fluctuations. HSYA also inhibited the increase of expression of the dopamine D3 receptor in the striatum.
    CONCLUSIONS:
    These findings demonstrated that HSYA provided anti-dyskinetic relief against Levodopa in a preclinical model of PD via regulating the expression of the dopamine D3 receptor. The combination of Levodopa and HSYA also reduced the likelihood of wearing off development, and may thus support the utility of such compounds for the improved treatment of PD.
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